Abstract

The observation that profound losses in neocortical cholinergic innervation (Davies and Maloney, 1976; Perry et al., 1978; Whitehouse et al., 1982; Coyle et al., 1983) occur in Alzheimer’s disease (AD) and data pointing to the importance of cholinergic function to learning and memory in animals (El-Defrawy et al, 1985; Watson et al. 1985, Hepler et al., 1985) have led to what has been called the cholinergic hypothesis of AD. This hypothesis states that the cholinergic losses observed in AD lead, at least in part, to the cognitive and mnemonic deficits observed in the disease. However, with the wide range of neurochemical alterations now documented in AD the cholinergic hypothesis appears to be an oversimplification (Price, 1986; D’Amato et al., 1987; Struble et al., 1987).